Skip to main content
SYS · ONLINEPASS · 63.0%
Open Assay
Independent Testing / Est. 2026
BATCH04·26·B
PASS63.0%
N27
PeptidesLongevityLiquid Glutathione

Liquid Glutathione

/ Reduced glutathione (GSH); endogenous tripeptide antioxidant (gamma-Glu-Cys-Gly)
TIER 2 · TranslationalN = 0 · TESTING PENDINGMW 307.32 g·mol⁻¹

ALIAS · Reduced glutathione · GSH · L-Glutathione (reduced)

Pass rate
0
Samples
0
Suppliers
Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

Terms in this page you can click for a plain-English popup: , , , , , , , .

§ A · Identity
Primary sequenceγ-ECG (γ-glutamyl-cysteine-glycine)
MW · 307.32CLASS · Reduced glutathione (GSH); endogenous tripeptide antioxidant (gamma-Glu-Cys-Gly)CATEGORY · Longevity

Tier 2. Small randomised trials of intravenous reduced glutathione in Parkinson disease (Sechi 1996, Schmitt 2015) and oral bioavailability comparisons across formulations (Allen 2011 review). Parenteral N-acetylcysteine is FDA-approved for acetaminophen overdose; parenteral and liposomal glutathione products themselves have a more limited and region-variable approval profile, with the US compounding regulatory status best described as ambiguous.

§ B · Mechanism of action

Reduced glutathione (GSH) is the gamma-glutamyl tripeptide gamma-Glu-Cys-Gly, the predominant intracellular thiol antioxidant present at millimolar concentrations in most tissues and the rate-limiting cofactor of glutathione peroxidase, glutathione S-transferases, and glutaredoxin systems. The reactive cysteine thiol is oxidised to the disulfide GSSG and recycled back to GSH by NADPH-dependent glutathione reductase, maintaining the cellular redox set point.

Systemic GSH does not cross the plasma membrane intact; tissue uptake of intact glutathione is limited and most cells synthesise GSH de novo from cysteine, glycine, and glutamate using gamma-glutamylcysteine ligase as the rate-limiting enzyme. Oral glutathione bioavailability is therefore controversial: the gut and liver hydrolyse the tripeptide and reassemble cysteine for hepatic resynthesis, with downstream tissue benefit driven principally by cysteine delivery rather than intact GSH transport. Liposomal and sublingual formulations have generated pharmacokinetic data suggesting modest improvements in oral exposure, but tissue-level bioavailability remains the clinically relevant unknown.

§ C · Human clinical evidence

Tier 2. Sechi and colleagues (1996) reported intravenous reduced glutathione 600 mg twice daily for 30 days improved disability scores in early-stage Parkinson disease in an open-label pilot. Schmitt and colleagues (2015) randomised 21 PD participants to IV glutathione versus placebo and observed only modest endpoint changes. Oral bioavailability comparisons (Allen and Bradley 2011 review) document the longstanding pharmacokinetic challenge.

§ D · Primary literature
PubMed8938817Sechi G et al.Reduced intravenous glutathione in the treatment of early Parkinson's disease · Progress in Neuro-Psychopharmacology and Biological Psychiatry · human-phase-2Open-label IV glutathione 600 mg twice daily for 30 days produced approximately 42% improvement in disability scores in untreated early Parkinson disease, sustained over a two-to-four-month observation period.Limitations: Open-label; small n; no concurrent placebo control.1996
PubMed26262996Schmitt B et al.Effects of N-acetylcysteine, oral glutathione (GSH) and a novel sublingual GSH formulation on oxidative stress markers in human volunteers · Redox Biology · human-phase-2A novel sublingual reduced glutathione formulation produced detectable plasma GSH increases in healthy volunteers, addressing the longstanding bioavailability concern with conventional oral GSH; oxidative stress marker shifts were small.Limitations: Pharmacokinetic and biomarker endpoints in healthy volunteers; not a disease-population trial.2015
PubMed21875351Allen J et al.Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers · The Journal of Alternative and Complementary Medicine · human-phase-2Four weeks of oral reduced glutathione 500 mg twice daily produced no significant change in plasma GSH, GSSG, GSH/GSSG ratio, or 8-isoprostane in healthy adults versus placebo.Limitations: Healthy-adult population; biomarker endpoints; conventional oral formulation (not liposomal).2011
§ F · Safety signal

Intravenous reduced glutathione is well-tolerated in published trial doses but is not an FDA-approved standalone product in the US. Allergic reactions and infusion-site irritation have been reported. Compounded parenteral glutathione has been implicated in FDA warnings about non-sterile compounding practices at specific facilities; sterility, endotoxin, and identity assurance vary substantially across compounding sources.

§ H · Regulatory status

Regulatory status

FDA status:
FDA-approved
Compounding:
Compounding eligibility ambiguous
§ I · Notable gaps and controversies

Long-term geroscience outcome data are sparse. Most enthusiasm rests on the central role of GSH in cellular redox biology rather than controlled trial demonstration of clinical benefit at the human aging or chronic-disease scale. The 'liquid' or IV framing common in vendor and clinic marketing is not interchangeable with oral supplementation in pharmacokinetic terms; vendor marketing frequently conflates the two evidence bases. Compounded glutathione for non-FDA-approved indications has been the subject of multiple FDA enforcement actions.